Physiology and Pathophysiology Flashcards

What physiological parameter best guides ECMO flow titration to ensure adequate oxygen delivery (DO2) in VA-ECMO?

Answer: Mixed venous oxygen saturation (SvO2) reflecting the balance between DO2 and VO2

SvO2 integrates oxygen delivery and consumption; a falling SvO2 indicates tissues are extracting more oxygen to compensate for inadequate delivery, signaling the need to increase ECMO flow or hemoglobin.

In neonatal ECMO for persistent pulmonary hypertension of the newborn (PPHN), what is the primary pathophysiological target?

Answer: Reducing pulmonary vascular resistance to enable transition from fetal to neonatal circulation

PPHN results from failure of the pulmonary vasculature to dilate at birth, maintaining high PVR that drives right-to-left shunting; ECMO buys time while strategies to reduce PVR (inhaled NO, alkalosis, oxygen) take effect.

How does increasing ECMO blood flow affect plasma-free hemoglobin levels?

Answer: Hemolysis increases with higher rpm as centrifugal pump shear stress rises proportionally

Centrifugal pump rpm and shear forces increase with flow; higher shear stress exceeds red cell membrane tolerance, causing progressive mechanical hemolysis that correlates with pump speed.

What is the physiological consequence of excessive negative inlet pressure (high suction) at the venous drainage cannula during ECMO?

Answer: Cavitation, hemolysis, and intermittent flow interruption as the right atrium collapses around the cannula

Excessive negative pressure causes the compliant right atrial wall to intermittently collapse over the drainage cannula (chatter), inducing cavitation, red cell destruction, and unstable pump flow.

Which mechanism best explains why patients with severe right heart failure on VA-ECMO may paradoxically develop pulmonary edema?

Answer: Improved RV unloading by ECMO increases pulmonary blood flow into the failing LV, which cannot accommodate the increased preload

When VA-ECMO decompresses the RV and restores pulmonary blood flow, a severely impaired LV that cannot empty adequately develops rising LVEDP transmitted back to the pulmonary capillaries, causing hydrostatic edema.

In ECMO-supported patients, why does targeting a higher hemoglobin (>10 g/dL) improve oxygen delivery more efficiently than increasing pump flow alone?

Answer: Oxygen content is linearly related to hemoglobin concentration; each g/dL increase augments DO2 proportionally without the adverse pressure effects of higher pump flow

Since DO2 = CO × CaO2 and CaO2 depends directly on hemoglobin, optimizing hemoglobin increases oxygen delivery without raising pump speed, which carries risks of hemolysis and afterload elevation.

What pathophysiological process underlies 'circuit thrombosis' in ECMO, and which laboratory value best predicts impending oxygenator failure?

Answer: Activation of contact pathway coagulation on synthetic surfaces producing fibrin-platelet thrombi; rising pre- to post-membrane pressure gradient predicts oxygenator failure

Blood contact with synthetic circuit surfaces activates Factor XII and the intrinsic pathway, building fibrin-platelet thrombi; as clot accumulates in the oxygenator, resistance rises and the transmembrane pressure gradient increases, signaling impending failure.